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INTRODUCTION AND EPIDEMIOLOGY

Headache is the fifth most common symptom presenting to the ED in the United States, with a total of 2.1 million visits per year.1 Overall, headaches affect people across all ethnic, geographic, and economic levels, with an estimated global prevalence of 47% in adults.2

PATHOPHYSIOLOGY

The brain parenchyma has no pain sensors.3 Early theories postulating vasoconstriction and rebound vasodilatation as the cause of migraine have been refuted.4 Numerous physiologic mechanisms play a role in the development of the various clinical headache syndromes. For example, occipital nerve irritation may lead to the development of occipital neuralgia.5 Similarly, headaches associated with disturbances in intracranial pressure (both high and low) are related to compression of, or traction on, pressure-sensitive structures in the meninges.6 The pathophysiologic mechanisms of other headache syndromes, such as migraine headaches, cluster headaches, and toxic and metabolic headaches, are less clear. Discussion of these mechanisms is beyond the scope of this chapter.

CLINICAL FEATURES

Most patients with headache have conditions that are painful but benign in etiology. Identifying those at high risk is the first step in management (Table 165-1). A high-risk cause for headache accounts for only 4% of all headaches but 10% to 14% of acute-onset ("thunderclap") headaches.7,8 Although headaches are typically classified as primary headaches when there is no underlying cause (such as migraine or cluster headaches) and secondary headaches if associated with an underlying cause (such as tumor, meningitis, or subarachnoid hemorrhage), this distinction is not clinically useful in the ED setting.

HISTORY

Patient Age

Patients >50 years of age, with a new or worsening headache, represent a high-risk group. The incidence of migraine, cluster, and tension headaches decreases with age, raising the likelihood of ominous pathology for older patients.9